Th.W. Lameris (Thomas)http://repub.eur.nl/ppl/2175/
List of Publicationsenhttp://repub.eur.nl/eur_signature.pnghttp://repub.eur.nl/
RePub, Erasmus University RepositoryForearm Venous Distensibility Predicts Successful Arteriovenous Fistulahttp://repub.eur.nl/pub/64176/
Thu, 01 Jun 2006 00:00:01 GMT<div>J.C. van der Linden</div><div>Th.W. Lameris</div><div>A.H. van den Meiracker</div><div>A.A. de Smet</div><div>P.J. Blankestijn</div><div>M.A. van den Dorpel</div>
Background: The success of a newly created arteriovenous fistula (AVF) depends on sufficient maturation of the forearm vein used. This maturation fails in up to 50%. We hypothesize that impairment of forearm venous distensibility, ie, the ability of veins to adjust to increased pressure, is related to AVF failure. Methods: Forearm venous distensibility was measured by using strain-gauge plethysmography in 27 patients with end-stage renal failure awaiting vascular access surgery; either AVF or graft (AVG) formation. Ultrasound duplex scanning of the upper-extremity circulation was performed 4 weeks before surgery. Failure to mature is defined as inability to use the AVF for hemodialysis within 8 weeks after surgery. Results: Venous distensibility in patients receiving an AVG (n = 10) was 0.44 ± 0.05 mL/mm Hg, and in patients receiving an AVF (n =17), 0.56 ± 0.04 mL/mm Hg (P = 0.2). Venous distensibility was 0.46 ± 0.03 mL/mm Hg in patients with an unsuccessful AVF (n = 9) and 0.66 ± 0.05 mL/mm Hg in patients with a successful AVF (n = 8; P = 0.003). All 7 patients with venous distensibility of 0.50 mL/mm Hg or less had a nonfunctional AVF (100%), whereas only 2 of 10 patients with venous distensibility greater than 0.50 mL/mm Hg had a nonfunctional AVF (20%; P = 0.002). No differences were found in arterial and venous luminal diameters between functional and nonfunctional AVFs. Conclusion: These preliminary results suggest that forearm venous distensibility is a predictor of AVF success, whereas luminal diameters are not. Measurement of venous distensibility may be helpful in choosing the most suitable access type for each individual patient, possibly improving access patency.Effects of hyperbaric treatment in cerebral air embolism on intracranial pressure, brain oxygenation, and brain glucose metabolism in the pighttp://repub.eur.nl/pub/66693/
Fri, 01 Apr 2005 00:00:01 GMT<div>R.A. van Hulst</div><div>J. Drenthen</div><div>J.J. Haitsma</div><div>Th.W. Lameris</div><div>G.H. Visser</div><div>J. Klein</div><div>B.F. Lachmann</div>
Objective: To evaluate the effects of hyperbaric oxygen treatment after cerebral air embolism on intracranial pressure, brain oxygenation, brain glucose/lactate metabolism, and electroencephalograph. Design: Prospective animal study. Setting: Hyperbaric chamber. Subjects: Eleven Landrace/Yorkshire pigs. Interventions: In 11 anesthetized pigs, intracranial pressure and brain oxygenation were measured with microsensor technology, brain glucose/lactate by microdialysis, and electroencephalograph by conventional methods. After injection of air into the internal carotid artery, animals were treated immediately (at 3 mins; t = 3) or at 60 mins (t = 60) with U.S. Navy Treatment Table 6 for 4.48 hrs. Results: At the end of hyperbaric oxygen treatment, intracranial pressure in the t = 60 group (39 ± 8 mm Hg) was significantly higher than in the t = 3 group (27 ± 6 mm Hg), brain oxygenation values for group t = 3 and t = 60 were 66 ± 14 and 52 ± 15 mm Hg, respectively (no significant difference from baseline), and there were no pathologic scores in the visually assessed electroencephalograph. However, there was a significant decrease in brain glucose and a significant increase in brain lactate in both groups at the end of the 5-hr study period. Conclusions: Hyperbaric oxygen treatment initiated at both 3 and 60 mins after embolization decreased the deleterious effects of cerebral air embolism on intracranial pressure and brain metabolism. Therefore, this model appears suitable to test the application of hyperbaric oxygen treatment with a delay >60 mins after embolization, as is often the case in the clinical situation. CopyrightSafety of perioperative statin use in high-risk patients undergoing major vascular surgeryhttp://repub.eur.nl/pub/54585/
Tue, 01 Mar 2005 00:00:01 GMT<div>O. Schouten</div><div>M.D. Kertai</div><div>J.J. Bax</div><div>A.E.S. Durazzo</div><div>E. Biagini</div><div>H. Boersma</div><div>V.H. van Waning</div><div>Th.W. Lameris</div><div>M.R.H.M. van Sambeek</div><div>D. Poldermans</div>
No clinical data are available on the influence of perioperative statin use on postoperative myopathy in patients undergoing major noncardiac surgery except for some case reports. Therefore, the aim of this study was to clarify the potential risk of myopathy in statin users who underwent major noncardiac surgery.Fluvastatin and bisoprolol for the reduction of perioperative cardiac mortality and morbidity in high-risk patients undergoing non-cardiac surgery: Rationale and design of the DECREASE-IV studyhttp://repub.eur.nl/pub/52837/
Wed, 01 Dec 2004 00:00:01 GMT<div>O. Schouten</div><div>D. Poldermans</div><div>L.E. Visser</div><div>M.D. Kertai</div><div>J. Klein</div><div>H. van Urk</div><div>M.L. Simoons</div><div>L.L.M. van de Ven</div><div>M. Vermeulen</div><div>J.J. Bax</div><div>Th.W. Lameris</div><div>H. Boersma</div>
Hyperventilation impairs brain function in acute cerebral air embolism in pigshttp://repub.eur.nl/pub/64920/
Sat, 01 May 2004 00:00:01 GMT<div>R.A. van Hulst</div><div>J.J. Haitsma</div><div>Th.W. Lameris</div><div>J. Klein</div><div>B.F. Lachmann</div>
Increased plasma concentration of natriuretic peptides by selective β1-blocker bisoprololhttp://repub.eur.nl/pub/60649/
Wed, 01 Oct 2003 00:00:01 GMT<div>A.H. van den Meiracker</div><div>Th.W. Lameris</div><div>L.L.M. van de Ven</div><div>F. Boomsma</div>
Exogenous angiotensin II does not facilitate norepinephrine release in the hearthttp://repub.eur.nl/pub/60928/
Tue, 01 Oct 2002 00:00:01 GMT<div>Th.W. Lameris</div><div>P.A. de Zeeuw</div><div>D.J.G.M. Duncker</div><div>G. Alberts</div><div>F. Boomsma</div><div>P.D. Verdouw</div><div>A.H. van den Meiracker</div>
Epinephrine in the heart: Uptake and release, but no facilitation of norepinephrine releasehttp://repub.eur.nl/pub/65959/
Tue, 13 Aug 2002 00:00:01 GMT<div>Th.W. Lameris</div><div>P.A. de Zeeuw</div><div>D.J.G.M. Duncker</div><div>W. Tietge</div><div>G. Alberts</div><div>F. Boomsma</div><div>P.D. Verdouw</div><div>A.H. van den Meiracker</div>
Epinephrine in the heart: uptake and release, but no facilitation of norepinephrine releasehttp://repub.eur.nl/pub/9953/
Tue, 01 Jan 2002 00:00:01 GMT<div>Th.W. Lameris</div><div>P.A. de Zeeuw</div><div>D.J.G.M. Duncker</div><div>W. Tietge</div><div>G. Alberts</div><div>F. Boomsma</div><div>P.D. Verdouw</div><div>A.H. van den Meiracker</div>
BACKGROUND: Several studies have suggested that epinephrine augments the
release of norepinephrine from sympathetic nerve terminals through
stimulation of presynaptic receptors, but evidence pertaining to this
mechanism in the heart is scarce and conflicting. Using the microdialysis
technique in the porcine heart, we investigated whether epinephrine, taken
up by and released from cardiac sympathetic nerves, can increase
norepinephrine concentrations in myocardial interstitial fluid (NE(MIF))
under basal conditions and during sympathetic activation. METHODS AND
RESULTS: During intracoronary epinephrine infusion of 10, 50, and 100
ng/kg per minute under basal conditions, large increments in interstitial
(from 0.31+/-0.05 up to 140+/-30 nmol/L) and coronary venous (from
0.16+/-0.08 up to 228+/-39 nmol/L) epinephrine concentrations were found,
but NE(MIF) did not change. Left stellate ganglion stimulation increased
NE(MIF) from 3.4+/-0.5 to 8.2+/-1.5 nmol/L, but again, this increase was
not enhanced by concomitant intracoronary epinephrine infusion.
Intracoronary infusion of tyramine resulted in a negligible increase in
epinephrine concentration in myocardial interstitial fluid (EPI(MIF)),
whereas 30 minutes after infusion of epinephrine an increase of 9.5 nmol/L
in EPI(MIF) was observed, indicating that epinephrine is taken up by and
released from cardiac sympathetic neurons. Although 68% to 78% of infused
epinephrine was extracted over the heart, the ratio of interstitial to
arterial epinephrine concentrations was only approximately 20%, increasing
to 29% with neuronal reuptake inhibition. CONCLUSIONS: Our findings
demonstrate epinephrine release from cardiac sympathetic neurons, but they
do not provide evidence that epinephrine augments cardiac sympathoneural
norepinephrine release under basal conditions or during sympathetic
activation.Exogenous angiotensin II does not facilitate norepinephrine release in the hearthttp://repub.eur.nl/pub/9991/
Tue, 01 Jan 2002 00:00:01 GMT<div>Th.W. Lameris</div><div>P.A. de Zeeuw</div><div>D.J.G.M. Duncker</div><div>G. Alberts</div><div>F. Boomsma</div><div>P.D. Verdouw</div><div>A.H. van den Meiracker</div>
Studies on the effect of angiotensin II on norepinephrine release from
sympathetic nerve terminals through stimulation of presynaptic angiotensin
II type 1 receptors are equivocal. Furthermore, evidence that angiotensin
II activates the cardiac sympathetic nervous system in vivo is scarce or
indirect. In the intact porcine heart, we investigated whether angiotensin
II increases norepinephrine concentrations in the myocardial interstitial
fluid (NE(MIF)) under basal conditions and during sympathetic activation
and whether it enhances exocytotic and nonexocytotic ischemia-induced
norepinephrine release. In 27 anesthetized pigs, NE(MIF) was measured in
the left ventricular myocardium using the microdialysis technique. Local
infusion of angiotensin II into the left anterior descending coronary
artery (LAD) at consecutive rates of 0.05, 0.5, and 5 ng/kg per minute did
not affect NE(MIF), LAD flow, left ventricular dP/dt(max), and arterial
pressure despite large increments in coronary arterial and venous
angiotensin II concentrations. In the presence of neuronal reuptake
inhibition and alpha-adrenergic receptor blockade, left stellate ganglion
stimulation increased NE(MIF) from 2.7+/-0.3 to 7.3+/-1.2 before, and from
2.3+/-0.4 to 6.9+/-1.3 nmol/L during, infusion of 0.5 ng/kg per minute
angiotensin II. Sixty minutes of 70% LAD flow reduction caused a
progressive increase in NE(MIF) from 0.9+/-0.1 to 16+/-6 nmol/L, which was
not enhanced by concomitant infusion of 0.5 ng/kg per minute angiotensin
II. In conclusion, we did not observe any facilitation of cardiac
norepinephrine release by angiotensin II under basal conditions and during
either physiological (ganglion stimulation) or pathophysiological (acute
ischemia) sympathetic activation. Hence, angiotensin II is not a local
mediator of cardiac sympathetic activity in the in vivo porcine heart.Microdialysis: Touching the fingertips of the cardiac sympathetic nervous systemhttp://repub.eur.nl/pub/23634/
Wed, 19 Dec 2001 00:00:01 GMT<div>Th.W. Lameris</div>
For years sympathetic activity in man and experimental animals has been
assessed by measuring circulating catecholamines. As their plasma
concentration is not only determined by sympathetic activity but also by
spillover and clearance, it is only useful as a screening tool for gross
disturbances in general sympathetic tone. The isotope dilution method uses
tritiated norepinephrine to differentiate between norepinephrine release into
and its removal from the circulation. This technique is not only more precise
but can also be applied for the assessment of regional sympathetic tone.
Alternatively, local sympathetic activity can be monitored by
microneurography, i.e. measuring the electrical activity of postganglionic
sympathetic efferents. However, due to its invasive nature, microneurography
in humans is restricted to monitoring sympathetic control of skin and muscle
vasculature. Microdialysis is a new technique that can monitor local
sympathetic act!Vlty almost continuously by measuring interstitial
norepinephrine concentrations. The technique is based on the diffusion of
norepinephrine from the intercellular space through a semi-permeable
membrane mounted in a small catheter into a suitable perfusion fluid like
Ringer's or Ringer's lactate, which can be collected continuously for later
analysis. In conclusion, none of the mentioned techniques for monitoring
sympathetic activity is superior to another as each has its own strengths and
limitations. The choice for one or more of these methods strongly depends on
the question that has to be answered; a combination of the various techniques
may provide the investigator with a more powerful tool to monitor the
sympathetic nervous system.Cardioprotection in pigs by exogenous norepinephrine but not by cerebral ischemia-induced release of endogenous norepinephrinehttp://repub.eur.nl/pub/9607/
Mon, 01 Jan 2001 00:00:01 GMT<div>P.A. de Zeeuw</div><div>Th.W. Lameris</div><div>D.J.G.M. Duncker</div><div>D. Hasan</div><div>F. Boomsma</div><div>A.H. van den Meiracker</div><div>P.D. Verdouw</div>
BACKGROUND AND PURPOSE: Endogenous norepinephrine release induced by
cerebral ischemia may lead to small areas of necrosis in normal hearts.
Conversely, norepinephrine may be one of the mediators that limit
myocardial infarct size by ischemic preconditioning. Because brief
ischemia in kidneys or skeletal muscle limits infarct size produced by
coronary artery occlusion, we investigated whether cardiac norepinephrine
release during transient cerebral ischemia also elicits remote myocardial
preconditioning. METHODS: Forty-one crossbred pigs of either sex were
assigned to 1 of 7 experimental groups, of which in 6 groups myocardial
infarct size was determined after a 60-minute coronary occlusion and 120
minutes of reperfusion. One group served as control (no pretreatment),
while the other groups were pretreated with either cerebral ischemia or an
intracoronary infusion of norepinephrine. RESULTS: In 10 anesthetized
control pigs, infarct size was 84+/-3% (mean+/-SEM) of the area at risk
after a 60-minute coronary occlusion and 120 minutes of reperfusion.
Intracoronary infusion of 0.03 nmol/kg. min(-)(1) norepinephrine for 10
minutes before coronary occlusion did not affect infarct size (80+/-3%;
n=6), whereas infusion of 0.12 nmol/kg. min(-)(1) limited infarct size
(65+/-2%; n=7; P:<0.05). Neither 10-minute (n=5) nor 30-minute (n=6)
cerebral ischemia produced by elevation of intracranial pressure before
coronary occlusion affected infarct size (83+/-4% and 82+/-3%,
respectively). Myocardial interstitial norepinephrine levels tripled
during cerebral ischemia and during low-dose norepinephrine but increased
10-fold during high-dose norepinephrine. Norepinephrine levels increased
progressively up to 500-fold in the area at risk during the 60-minute
coronary occlusion, independent of the pretreatment, while norepinephrine
levels remained unchanged in adjacent nonischemic myocardium and arterial
plasma. CONCLUSIONS: Cerebral ischemia preceding a coronary occlusion did
not modify infarct size, which is likely related to the modest increase in
myocardial norepinephrine levels during cerebral ischemia. The infarct
size limitation by high-dose exogenous norepinephrine is not associated
with blunting of the ischemia-induced increase in myocardial interstitial
norepinephrine levels.Time Course and Mechanism of Myocardial Catecholamine Release During Transient Ischemia In Vivohttp://repub.eur.nl/pub/9379/
Sat, 01 Jan 2000 00:00:01 GMT<div>Th.W. Lameris</div><div>P.A. de Zeeuw</div><div>G. Alberts</div><div>F. Boomsma</div><div>D.J.G.M. Duncker</div><div>P.D. Verdouw</div><div>A.H. van den Meiracker</div><div>A.J. Man in 't Veld</div>
BACKGROUND: Elevated concentrations of norepinephrine (NE) have been
observed in ischemic myocardium. We investigated the magnitude and
mechanism of catecholamine release in the myocardial interstitial fluid
(MIF) during ischemia and reperfusion in vivo through the use of
microdialysis. METHODS AND RESULTS: In 9 anesthetized pigs, interstitial
catecholamine concentrations were measured in the perfusion areas of the
left anterior descending coronary artery (LAD) and the left circumflex
coronary artery. After stabilization, the LAD was occluded for 60 minutes
and reperfused for 150 minutes. During the final 30 minutes, tyramine (154
nmol. kg(-1). min(-1)) was infused into the LAD. During LAD occlusion, MIF
NE concentrations in the ischemic region increased progressively from 1.
0+/-0.1 to 524+/-125 nmol/L. MIF concentrations of dopamine and
epinephrine rose from 0.4+/-0.1 to 43.9+/-9.5 nmol/L and from <0.2
(detection limit) to 4.7+/-0.7 nmol/L, respectively. Local uptake-1
blockade attenuated release of all 3 catecholamines by >50%. During
reperfusion, MIF catecholamine concentrations returned to baseline within
120 minutes. At that time, the tyramine-induced NE release was similar to
that seen in nonischemic control animals despite massive infarction.
Arterial and MIF catecholamine concentrations in the left circumflex
coronary artery region remained unchanged. CONCLUSIONS: Myocardial
ischemia is associated with a pronounced increase of MIF catecholamines,
which is at least in part mediated by a reversed neuronal reuptake
mechanism. The increase of MIF epinephrine implies a (probably neuronal)
cardiac source, whereas the preserved catecholamine response to tyramine
in postischemic necrotic myocardium indicates functional integrity of
sympathetic nerve terminals.Sensitive and specific method for the simultaneous determination of natural and synthetic catecholamines and 3,4-dihydroxyphenylglycol in microdialysis sampleshttp://repub.eur.nl/pub/63803/
Fri, 09 Jul 1999 00:00:01 GMT<div>G. Alberts</div><div>Th.W. Lameris</div><div>A.H. van den Meiracker</div><div>A.J. Man in't Veld</div><div>F. Boomsma</div>
Catecholamine handling in the porcine heart: a microdialysis approachhttp://repub.eur.nl/pub/9176/
Fri, 01 Jan 1999 00:00:01 GMT<div>Th.W. Lameris</div><div>A.H. van den Meiracker</div><div>F. Boomsma</div><div>G. Alberts</div><div>P.A. de Zeeuw</div><div>D.J.G.M. Duncker</div><div>P.D. Verdouw</div><div>A.J. Man in 't Veld</div>
Experimental findings suggest a pronounced concentration gradient of
norepinephrine (NE) between the intravascular and interstitial
compartments of the heart, compatible with an active neuronal reuptake
(U1) and/or an endothelial barrier. Using the microdialysis technique in
eight anesthetized pigs, we investigated this NE gradient, both under
baseline conditions and during increments in either systemic or myocardial
interstitial fluid (MIF) NE concentration. At steady state, baseline MIF
NE (0.9 +/- 0.1 nmol/l) was higher than arterial NE (0.3 +/- 0.1 nmol/l)
but was not different from coronary venous NE (1.5 +/- 0.3 nmol/l). Local
U1 inhibition raised MIF NE concentration to 6.5 +/- 0.9 nmol/l. During
intravenous NE infusions (0.6 and 1.8 nmol. kg(-1). min(-1)), the
fractional removal of NE by the myocardium was 79 +/- 4% to 69 +/- 3%,
depending on the infusion rate. Despite this extensive removal, the
quotient of changes in MIF and arterial concentration (DeltaMIF/DeltaA
ratio) for NE were only 0.10 +/- 0.02 for the lower infusion rate and 0.11
+/- 0.01 for the higher infusion rate, whereas U1 blockade caused the
DeltaMIF/DeltaA ratio to rise to 0.21 +/- 0.03 and 0.36 +/- 0.05,
respectively. From the differences in DeltaMIF/DeltaA ratios with and
without U1 inhibition, we calculated that 67 +/- 5% of MIF NE is removed
by U1. Intracoronary infusion of tyramine (154 nmol. kg(-1). min(-1))
caused a 15-fold increase in MIF NE concentration. This pronounced
increase was paralleled by a comparable increase of NE in the coronary
vein. We conclude that U1 and extraneuronal uptake, and not an endothelial
barrier, are the principal mechanisms underlying the concentration
gradient of NE between the interstitial and intravascular compartments in
the porcine heart.Forearm vasorelaxation in hypertensive renal transplant patients: The impact of withdrawal of cyclosporinehttp://repub.eur.nl/pub/68622/
Wed, 18 Mar 1998 00:00:01 GMT<div>M.A. van den Dorpel</div><div>A.H. van den Meiracker</div><div>Th.W. Lameris</div><div>W. Weimar</div><div>A.J. Man in't Veld</div>